Effect of an increase in systemic blood pressure on nailfold capillary pressure in humans

1993 ◽  
Vol 265 (3) ◽  
pp. H820-H823 ◽  
Author(s):  
A. C. Shore ◽  
D. D. Sandeman ◽  
J. E. Tooke
Keyword(s):  
Blood Pressure ◽  
Capillary Pressure ◽  
Venous Pressure ◽  
Isometric Exercise ◽  
Systemic Blood Pressure ◽  
Isometric Handgrip ◽  
Systemic Blood ◽  
Protective Mechanisms ◽  
Arterial Blood ◽  
Contralateral Hand

Moderate autoregulation of capillary pressure occurs during changes in arterial and/or venous pressure in animals. Whether an increase in systemic blood pressure is transmitted to capillaries in humans is unknown. Eight healthy volunteers performed isometric handgrip exercise (30% of maximum) while nailfold capillary pressure (CP) and digital arterial blood pressure (DBP) were measured in the contralateral hand. CP was measured for 40 s before exercise and 40-100 s during exercise. Only experiments with no change in pipette position and no artifactual changes in flow were accepted. Basal DBP was stable [91.5 +/- 12.7 mmHg (-40 to -20 s basal) and 91.3 +/- 11.8 mmHg (-20 to 0 s basal)], and isometric exercise increased DBP [100.4 +/- 13.9 mmHg (0-20 s exercise) and 103.1 +/- 15.3 mmHg (20-40 s exercise); P < 0.05]. CP was unchanged during the first 40 s of exercise [18.9 +/- 4.9 mmHg (-40 to 20 s basal), 18.9 +/- 5.2 mmHg (-20 to 0 s basal), 18.4 +/- 4.7 mmHg (0-20 s exercise), and 18.3 +/- 5.3 mmHg (20-40 s exercise)] and remained unchanged for up to 100 s (n = 5), despite a continued elevation of DBP. These data suggest that protective mechanisms minimize the transmission of increases in systemic blood pressure to the capillary bed in humans.

Influence of Sympatholytic Drugs on the Cardiovascular Response to Isometric Exercise

1981 ◽  
Vol 60 (2) ◽  
pp. 139-143 ◽  
Author(s):  
S. J. Watt ◽  
R. D. Thomas ◽  
P. W. Belfield ◽  
P. W. Goldstraw ◽  
S. H. Taylor
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Healthy Subjects ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Isometric Exercise ◽  
Systemic Blood Pressure ◽  
Isometric Handgrip ◽  
Systemic Blood ◽  
Oral Doses

1. The effects of single oral doses of various sympatholytic drugs on the heart rate and blood pressure increases during isometric handgrip contraction were studied in six healthy subjects. 2. Bethanidine reduced both the systolic and diastolic increases in pressure. Clonidine reduced the systolic but not the diastolic increase. Oxprenolol alone or in combination with phentolamine or phenyoxybenzamine failed to influence the pressor response. 3. The increase in systemic blood pressure associated with sustained contraction of voluntary muscle appears to be relatively resistant to acute sympathetic adrenoreceptor blockade in man.

Effects of systemic arterial blood pressure on the contractile force of a human hand muscle

2000 ◽  
Vol 88 (4) ◽  
pp. 1390-1396 ◽  
Author(s):  
Julie R. Wright ◽  
D. I. McCloskey ◽  
Richard C. Fitzpatrick
Keyword(s):  
Blood Pressure ◽  
Muscular Activity ◽  
Systemic Blood Pressure ◽  
Muscle Performance ◽  
Knee Extensors ◽  
Human Hand ◽  
Physiological Changes ◽  
Force Output ◽  
Systemic Blood ◽  
Arterial Blood

The effect of physiological changes in systemic blood pressure on the force output of working abductor pollicis (AP) muscle was studied in six normal subjects. Supramaximal tetanic stimulation at the ulnar nerve produced repeated isometric contractions at 1-s intervals. Force output declined gradually with time. During the train of contractions, subjects voluntarily contracted the knee extensors for 1 min; this raised systemic blood pressure by 29%. Force output from AP rose in parallel with blood pressure so that 18% of the contraction force lost through fatigue was recovered for each 10% increase in blood pressure. When blood pressure in the hand was kept constant despite the increased systemic pressure, force output did not rise. The results show that muscle performance is strongly affected by physiological changes in central blood pressure and suggest that sensory input concerning the adequacy of muscle performance exerts a feedback control over the increase in systemic blood pressure during muscular activity.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Sympathoadrenal-circulatory regulation during sustained isometric exercise in young and older men

1991 ◽  
Vol 261 (5) ◽  
pp. R1061-R1069 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Vascular Resistance ◽  
Isometric Exercise ◽  
Older Men ◽  
Electromyographic Activity ◽  
Isometric Handgrip ◽  
Significant Group ◽  
Arterial Blood ◽  
Older Subjects

The aim of this study was to test the hypothesis that the arterial blood pressure, vasoconstrictor, and sympathoadrenal adjustments to sustained submaximal isometric exercise become augmented with advancing age in humans. Fourteen young (26 +/- 1 yr) and 14 older (66 +/- 1 yr) healthy males performed isometric handgrip exercise at 30% of maximal voluntary force until exhaustion (inability to maintain target force). Maximal handgrip force was quite similar in the young and older subjects (402 +/- 20 vs. 392 +/- 20 N, respectively). The two groups did not differ significantly on any variable at rest. During sustained handgrip to exhaustion, peak levels of both perceived exertion and contracting forearm electromyographic activity were similar in the young and older men, suggesting equivalent voluntary efforts. Exercise time was not different in the two groups (315 +/- 27 s in young vs. 339 +/- 17 s in older men). Throughout exercise the increases in arterial blood pressure were very similar in the young and older subjects. Heart rate increased less (P less than 0.05), but stroke volume (impedance cardiography) tended to decrease less (not significant) in the older men; thus the increases in cardiac output were not different in the two groups. During the latter portion of exercise, systemic vascular resistance tended to increase in both the young and older men, with no significant group differences. The blood flow responses in the whole calf (venous occlusion plethysmography) and the calf skin (laser-Doppler velocimetry) were similar in the young and older subjects, as were the corresponding increases in vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Site and mechanism for compression of the venous system during experimental intracranial hypertension

1974 ◽  
Vol 41 (4) ◽  
pp. 427-434 ◽  
Author(s):  
Yoku Nakagawa ◽  
Mitsuo Tsuru ◽  
Kenzoh Yada
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Pressure Gradient ◽  
Superior Sagittal Sinus ◽  
Venous Pressure ◽  
Systemic Blood Pressure ◽  
Intraluminal Pressure ◽  
Systemic Blood ◽  
Sagittal Sinus ◽  
Bridging Vein

✓ The pressure gradient of the venous pathway between the cortical vein and superior sagittal sinus was measured in adult mongrel dogs by recording the pressures of the bridging vein, lateral lacuna (proximal portion), and superior sagittal sinus, together with the systemic blood pressure while gradually increasing the intracranial pressure up to the level of mean systemic blood pressure. The pressure gradient between the lateral lacuna and the superior sagittal sinus was also measured under increased intracranial pressure. Pressures of the bridging vein and lateral lacuna were constantly 50 to 250 mm H2O higher than the intracranial pressure, regardless of the level of intracranial pressure. An abrupt drop in the intraluminal pressure was observed at a point 1 to 2 mm proximal to the junction of the lateral lacuna and the superior sagittal sinus, regardless of the level of intracranial pressure. It is concluded that gradual stenosis of the parasagittal venous pathways took place 1 to 2 mm proximal to the junction between the lacuna and the superior sagittal sinus, and thus cortical venous pressure was maintained 50 to 250 mm H2O higher than intracranial pressure. The authors believe that an “intracranial venous pressure regulation mechanism” exists at the junction of the lateral lacuna and the superior sagittal sinus.

scholarly journals Endothelial cell regulation of systemic haemodynamics and metabolism acts through the HIF transcription factors

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Simon Lambden ◽  
Andrew S. Cowburn ◽  
David Macias ◽  
Tessa A. C. Garrud ◽  
Bernardo J. Krause ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Metabolic Rate ◽  
Vascular Endothelium ◽  
Vascular Function ◽  
Acute Stress ◽  
Acute Hypoxia ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Pulmonary Endothelium ◽  
Arterial Blood

Abstract Background The vascular endothelium has important endocrine and paracrine roles, particularly in the regulation of vascular tone and immune function, and it has been implicated in the pathophysiology of a range of cardiovascular and inflammatory conditions. This study uses a series of transgenic murine models to explore for the first time the role of the hypoxia-inducible factors, HIF-1α and HIF-2α in the pulmonary and systemic circulations as potential regulators of systemic vascular function in normoxic or hypoxic conditions and in response to inflammatory stress. We developed a series of transgenic mouse models, the HIF-1α Tie2Cre, deficient in HIF1-α in the systemic and pulmonary vascular endothelium and the L1Cre, a pulmonary endothelium specific knockout of HIF-1α or HIF-2α. In vivo, arterial blood pressure and metabolic activity were monitored continuously in normal atmospheric conditions and following an acute stimulus with hypoxia (10%) or lipopolysaccharide (LPS). Ex vivo, femoral artery reactivity was assessed using wire myography. Results Under normoxia, the HIF-1α Tie2Cre mouse had increased systolic and diastolic arterial pressure compared to litter mate controls over the day–night cycle under normal environmental conditions. VO2 and VCO2 were also increased. Femoral arteries displayed impaired endothelial relaxation in response to acetylcholine mediated by a reduction in the nitric oxide dependent portion of the response. HIF-1α L1Cre mice displayed a similar pattern of increased systemic blood pressure, metabolic rate and impaired vascular relaxation without features of pulmonary hypertension, polycythaemia or renal dysfunction under normal conditions. In response to acute hypoxia, deficiency of HIF-1α was associated with faster resolution of hypoxia-induced haemodynamic and metabolic compromise. In addition, systemic haemodynamics were less compromised by LPS treatment. Conclusions These data show that deficiency of HIF-1α in the systemic or pulmonary endothelium is associated with increased systemic blood pressure and metabolic rate, a pattern that persists in both normoxic conditions and in response to acute stress with potential implications for our understanding of the pathophysiology of vascular dysfunction in acute and chronic disease.

Brain adenosine production in rat during sustained alteration in systemic blood pressure

1980 ◽  
Vol 239 (5) ◽  
pp. H636-H641 ◽  
Author(s):  
H. R. Winn ◽  
J. E. Welsh ◽  
R. Rubio ◽  
R. M. Berne
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Autoregulation ◽  
Adenine Nucleotides ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Severe Hypotension

Brain production of adenosine and its metabolites, inosine and hypoxanthine was determined in 46 rats during sustained (5 min) reduction in mean arterial blood pressure (MABP) caused by hemorrhage. Also measured were ATP, ADP, AMP, phosphocreatine (PCr), and lactate. Brain tissue was obtained by the freeze-blowing technique. Ventilation was controlled to maintain constant arterial O2 tension, CO2 tension, and pH. When MABP was decreased from 135 + 3 (SE) mmHg to 72 +/- 2 mmHg, within the range of cerebral autoregulation, brain adenosine concentration doubled from 0.55 +/- 0.12 to 1.16 +/- 0.13 nmol/g (P < 0.015). Unlike the changes in adenosine concentrations, adenine nucleotides and PCr remained stable. Lactate varied inversely with MABP. With moderate to severe hypotension (MABP = 45 +/- 3 mmHg), adenosine levels increased almost sixfold. The increment in brain adenosine concentration within the autoregulatory range supports a role for this potent dilator of pial vessels in the regulation of cerebral blood flow.

Abstract P617: Actions on the Splanchnic Venous System Contribute to 5-HT-induced Hypotension

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Bridget M Seitz ◽  
Teresa Krieger-Burke ◽  
Hannah Garver ◽  
Gregory D Fink ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Portal Vein ◽  
Receptor Antagonist ◽  
Portal Pressure ◽  
Vena Cava ◽  
Systemic Blood Pressure ◽  
Venous System ◽  
Systemic Blood ◽  
Induced Hypotension ◽  
Arterial Blood

Infusion of serotonin (5-hydroxytryptamine, 5-HT) into conscious normotensive and hypertensive rats causes a sustained reduction in systemic blood pressure. Imaging studies reveal that the blood pressure fall is closely associated with dilation of the large splanchnic veins (mesenteric, portal and abdominal vena cava), suggesting that active venodilation contributes to the fall in blood pressure. In fact, isolated splanchnic veins dilate directly to 5-HT via activation of the 5-HT 7 receptor, and a 5-HT 7 receptor antagonist prevents the 5-HT induced fall in blood pressure. To determine if the splanchnic venodilation caused by 5-HT is active or passive, anesthetized male Sprague Dawley rats were instrumented with arterial and venous lines for pressure measurements and 5-HT administration, respectively, while splanchnic veins were imaged using the Vevo® 2100 Ultrasound system. Measures were made relative to baselines measures. Within 5 minutes of infusion, 5-HT (25 ug/kg/min) caused an initial fall in portal vein pressure (~8-10% reduction) accompanied by dilation of the portal vein (~40% increase). No changes were seen in the dimensions or pressure of the abdominal vena cava at this time. Mean arterial blood pressure was reduced (>40% reduction). All of these changes were prevented by pretreatment with the 5-HT 7 receptor antagonist SB269970. SB269970 during 5-HT infusion also caused an immediate reversal of changes in blood pressure and venous dimensions. Thus, active dilation of the pre-hepatic splanchnic venous system may be an early cause of 5-HT-induced hypotension. A more chronic experiment was performed in rats that were instrumented with a new dual channel radiotelemeter for concomitant measure of systemic and portal pressure in the conscious state. Within one hour after initiation of 5-HT infusion, portal venous pressure was elevated 38±0.2% above baseline (n=3) versus vehicle infused animals (4±0.3% above baseline; n=3), suggesting an action of 5-HT on intrahepatic venous resistance. Within 24 hours, portal pressure elevation resolved but blood pressure remained reduced. Collectively these data highlight the portal venous circulation as an important site of action for 5-HT in causing acute and chronic falls in systemic blood pressure.

Pericardial concentrations of adenosine, inosine and hypoxanthine in an experimental canine model of spastic ischaemia

2002 ◽  
Vol 103 (s2002) ◽  
pp. 198S-201S ◽  
Author(s):  
Violetta KÉKESI ◽  
Endre ZIMA ◽  
Erzsébet BARÁT ◽  
Éva HUSZÁR ◽  
Andrea NAGY ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Coronary Spasm ◽  
Systemic Blood Pressure ◽  
Canine Model ◽  
Pericardial Fluid ◽  
Metabolic Adaptation ◽  
Systemic Blood ◽  
Arterial Blood ◽  
Adenosine Concentration ◽  
Experimental Canine

It has been shown that the adenosine concentration in the pericardial fluid of the normal heart is higher by one order of magnitude than that of the venous plasma. A further increase in the pericardial adenosine concentration was also demonstrated in myocardial ischaemia or hypoxia. It was proposed that pericardial nucleoside levels may represent the interstitial concentrations of the adenine nucleosides. An experimental model was designed to determine the intrapericardial concentrations of adenosine, inosine and hypoxanthine during coronary spasm provoked by intracoronary administration of endothelin-1 (ET-1; 0.08±0.02nmol/g of myocardial tissue). In the in situ dog heart (n = 10), adenosine, inosine and hypoxanthine concentrations were determined by HPLC in fluid samples collected from the closed pericardial sac before and after ET-1 administration, and from the systemic arterial blood. Systemic blood pressure, heart rate and standard ECG were registered continuously. We found that the nucleoside concentrations in the infusate samples increased significantly during coronary spasm [adenosine, 1.49±0.44 compared with 0.37±0.07µM (P<0.05); inosine, 27.43±11.51 compared with 0.47±0.11µM (P<0.05); hypoxanthine, 21.17±6.49 compared with 4.91±1.24µM (P<0.05)], while a significant decrease in blood pressure and an elevation in ECG ST segments were observed. The levels of the purine metabolites did not change in the systemic blood. The data indicate that changes in adenine nucleoside levels measured in pericardial infusate samples reflect activation of coronary metabolic adaptation in this model of spastic ischaemia, and that pericardial nucleoside levels may characterize alterations in interstitial adenine nucleoside concentrations.

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